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16 results on '"Olukemi K Amodu"'

1. Sickle cell trait is associated with controlled levels of haem and mild proinflammatory response during acute malaria infection

Author

Olukemi K. Amodu, Gordon A. Awandare, and Temitope W. Ademolue

Subjects
Male, 0301 basic medicine, Hemoglobins, 0302 clinical medicine, Genotype, polycyclic compounds, Immunology and Allergy, Malaria, Falciparum, media_common, biology, Convalescence, Translational, digestive, oral, and skin physiology, 3. Good health, Child, Preschool, Toxicity, Cytokines, Original Article, Female, Infection, media_common.quotation_subject, Plasmodium falciparum, Immunology, malaria, Heme, Sickle Cell Trait, Proinflammatory cytokine, 03 medical and health sciences, parasitic diseases, medicine, Humans, haemoxygenase‐1, Inflammation, Sickle cell trait, business.industry, haem, Infant, Original Articles, medicine.disease, biology.organism_classification, 030104 developmental biology, Hemoglobin, business, Heme Oxygenase-1, Malaria, 030215 immunology
Abstract

Summary The controlled induction of haemoxygenase-1 (HO-1), an enzyme that catabolizes haem, has been shown to reduce haem, preventing pathologies associated with haem toxicity. The hemoglobin genotype HbAS confers reduced susceptibility to severe complications of malaria by a mechanism that is not well understood. Using a longitudinal approach, we investigated the effect of baseline concentrations of HO-1 on the accumulation of haem during acute Plasmodium falciparum malaria in HbAS and HbAA genotypes. Plasma concentrations of haem, HO-1 and cytokines were quantified in venous blood obtained from children (9 months–5 years of age) during malaria infection, and at convalescence (baseline levels). Parasitaemia was determined during malaria infection. In patients with the HbAA genotype, there was a significant elevation in the plasma concentration of haem (P = 0.002), and a consequent increased induction of HO-1 (P

Published
2017

2. New insights into malaria susceptibility from the genomes of 17,000 individuals from Africa, Asia, and Oceania

Author

Kate Rowlands, Timothy M. E. Davis, Salimata Konate, Umberto D'Alessandro, Angeliki Kerasidou, Sodiomon B. Sirima, David J. Conway, Fatoumatta Sisay-Joof, S Ademola, Mahamadou A. Thera, Momodou W. Jallow, Edith C. Bougouma, Alexander J. Mentzer, Alphaxard Manjurano, Chris Drakeley, Carolyne M. Ndila, Giorgio Sirugo, Eleanor Drury, Nguyen Hoan Phu, Moses Laman, Anthony Enimil, Pascal Michon, N T Ngoc Quyen, Terrie E. Taylor, Jennifer Evans, Ogobara K. Doumbo, Anita Ghansah, Malcolm E. Molyneux, Alexander T. Dilthey, Sibiry Sissoko, Olukemi K. Amodu, Kalifa Bojang, Yik Ying Teo, Ousmane Touré, Eleanor M. Riley, Dominic P. Kwiatkowski, Angela Allen, Laurens Manning, D Ansong, Peter Siba, Stephen Allen, Thomas N. Williams, Christina Hubbart, Tobias O. Apinjoh, Cao Quang Thai, Hugh Reyburn, Q S Le, Melanie Bahlo, Geraldine M. Clarke, Spencer Cca., Ivo Mueller, Anna E. Jeffreys, Gil McVean, Valentina D. Mangano, Jj J. Farrar, Victoria Cornelius, Busby Gbj., Kevin Marsh, Jim Stalker, David Modiano, Tran Tinh Hien, Michael T. Wilson, Tsiri Agbenyega, A Hodgson, Sarah J. Dunstan, Harin Karunajeewa, L. Amenga-Etego, Ellen M. Leffler, Katja Kivinen, Eric A. Achidi, Kirk A. Rockett, Kwadwo A. Koram, and J Shelton

Subjects
Genetics, Host resistance, biology, Plasmodium falciparum, Disease, Heritability, Hla association, biology.organism_classification, medicine.disease, Genome, Cerebral Malaria, parasitic diseases, medicine, Malaria
Abstract

We conducted a genome-wide association study of host resistance to severePlasmodium falciparummalaria in over 17,000 individuals from 11 malaria-endemic countries, undertaking a wide ranging analysis which identifies five replicable associations with genome-wide levels of evidence. Our findings include a newly implicated variant on chromosome 6 associated with risk of cerebral malaria, and the discovery of an erythroid-specific transcription start site underlying the association inATP2B4. Previously reported HLA associations cannot be replicated in this dataset. We estimate substantial heritability of severe malaria (h2~ 23%), of which around 10% is explained by the currently identified associations. Our dataset will provide a major building block for future research on the genetic determinants of disease in these diverse human populations.

Published
2019

3. Reappraisal of known malaria resistance loci in a large multicenter study

Author

Malcolm E. Molyneux, Peter Siba, Andre Ndi, Valentina D. Mangano, Cao Quang Thai, Vysaul Nyirongo, Subulade A. Olaniyan, Angie Green, Mahamadou A. Thera, Timothy M. E. Davis, Síle F. Molloy, Kathryn Fitzpatrick, Giorgio Sirugo, Edith C. Bougouma, Chris Drakeley, Anthony Enimil, Angela Allen, Olukemi K. Amodu, Christina Hubbart, Nuno Sepúlveda, Nguyen Hoan Phu, M Jallow, Carolyne M. Ndila, Stanley Usen, Kimberly J. Johnson, Hugh Reyburn, Taane G. Clark, Dominic P. Kwiatkowski, Si Quang Le, Tobias O. Apinjoh, Kalifa Bojang, Jennifer R Evans, Michael D. Wilson, Lee Hart, Sophie Uyoga, Angeliki Kerasidou, Eric A. Achidi, Steve Allen, Kirk A. Rockett, Pascal Michon, Ivo Mueller, Anna E. Jeffreys, Belco Poudiougou, Anita Ghansah, Norbert Peshu, Fatoumatta Sisay-Joof, David Kachala, Sodiomon B. Sirima, David J. Conway, Geraldine M. Clarke, Regina N. Mugri, Moses Laman, Aaron Vanderwal, Miguel A. Sanjoaquin, Sibiry Sissoko, Ousmane Touré, Laurens Manning, Chris C. A. Spencer, Matti Pirinen, David Modiano, Sarah J. Dunstan, Harin Karunajeewa, Alexander Macharia, Tran Tinh Hien, Tsiri Agbenyega, Gavin Band, Kate Rowlands, Salimata Konate, Rachel Craik, L. Amenga-Etego, Nguyen Ngoc Quyen, Kwadwo A. Koram, Amadou Niangaly, Margaret Pinder, Alphaxard Manjurano, Terrie E. Taylor, Ogobara K. Doumbo, Eleanor M. Riley, Jeremy Farrar, Victoria Cornelius, Kevin Marsh, and Thomas N. Williams

Subjects
medicine.medical_specialty, Genome-wide association study, Glucosephosphate Dehydrogenase, Polymorphism, Single Nucleotide, Article, Papua New Guinea, Plasma Membrane Calcium-Transporting ATPases, Polymorphism (computer science), ABO blood group system, parasitic diseases, Epidemiology, Genetics, medicine, Humans, Malaria, Falciparum, Africa South of the Sahara, Genetic Association Studies, Disease Resistance, biology, Transmission (medicine), Case-control study, Plasmodium falciparum, medicine.disease, biology.organism_classification, 3. Good health, Glucosephosphate Dehydrogenase Deficiency, Logistic Models, Vietnam, Genetic Loci, Case-Control Studies, Malaria
Abstract

Many human genetic associations with resistance to malaria have been reported, but few have been reliably replicated. We collected data on 11,890 cases of severe malaria due to Plasmodium falciparum and 17,441 controls from 12 locations in Africa, Asia and Oceania. We tested 55 SNPs in 27 loci previously reported to associate with severe malaria. There was evidence of association at P < 1 × 10(-4) with the HBB, ABO, ATP2B4, G6PD and CD40LG loci, but previously reported associations at 22 other loci did not replicate in the multicenter analysis. The large sample size made it possible to identify authentic genetic effects that are heterogeneous across populations or phenotypes, with a striking example being the main African form of G6PD deficiency, which reduced the risk of cerebral malaria but increased the risk of severe malarial anemia. The finding that G6PD deficiency has opposing effects on different fatal complications of P. falciparum infection indicates that the evolutionary origins of this common human genetic disorder are more complex than previously supposed.

Published
2014

4. Killer-cell immunoglobulin-like receptors and falciparum malaria in southwest Nigeria

Author

David J. Conway, Subulade A. Olaniyan, Louis-Marie Yindom, Peter Aka, Adekunle A. Bakare, O. O. Omotade, and Olukemi K. Amodu

Subjects
Male, Genotype, Plasmodium falciparum, Immunology, Population, Gene Expression, Nigeria, chemical and pharmacologic phenomena, Human leukocyte antigen, Severity of Illness Index, Asymptomatic, Interferon-gamma, Gene Frequency, Receptors, KIR, parasitic diseases, medicine, Humans, Immunology and Allergy, Malaria, Falciparum, education, Receptor, Alleles, education.field_of_study, biology, Infant, General Medicine, biology.organism_classification, medicine.disease, Virology, Killer Cells, Natural, Receptors, KIR2DL5, Child, Preschool, Asymptomatic Diseases, biology.protein, Female, medicine.symptom, Antibody, Malaria
Abstract

Killer-cell immunoglobulin-like receptors (KIRs) are a group of natural killer cell receptors (NKRs) that regulate NK-cell-mediated production of interferon gamma (IFN-γ) in response to infection. These receptors have recently been suggested to influence the severity of clinical Plasmodium falciparum malaria infection. We examined the KIR locus in relation to malaria in children from southwest Nigeria. Sequence specific priming (SSP)-PCR was used to detect the KIR genes. The presence or absence of fifteen different KIR genes was determined in each individual and the proportions compared across 3 clinical groups; asymptomatic malaria, uncomplicated clinical malaria and severe clinical malaria. The genes KIR2DL5, KIR2DS3 and KIR2DS5 were present in a significantly higher proportion of individuals in the asymptomatic control group than in the malaria cases. Furthermore, KIR2DS3 and KIR2DS5 were present in a higher proportion of uncomplicated malaria cases than severe malaria cases. Carriage c-AB2 genotype (which comprises all centromeric KIR genes including KIR2DL5, KIR2DS3 and KIR2DS5) decreases with severity of the disease suggesting that the KIR AB profile might be associated with protection from severe malaria infection in this population in Nigeria.

Published
2014

5. Relationship of Host Genetic Factors with Severe Malaria in Nigerian Children

Author

Victor R. Gordeuk, Binal N. Shah, Bamidele O. Tayo, Subulade Abigail Ademola, and Olukemi K. Amodu

Subjects
Sickle cell trait, medicine.medical_specialty, biology, business.industry, Anemia, Immunology, Plasmodium falciparum, Cell Biology, Hematology, Odds ratio, medicine.disease, biology.organism_classification, Biochemistry, Sickle cell anemia, Cerebral Malaria, Internal medicine, parasitic diseases, Medicine, business, Malaria, Glucose-6-phosphate dehydrogenase deficiency
Abstract

Host genetic factors that influence the outcome of Plasmodium falciparum malaria infection are not fully understood. These include alpha-thalassemia, sickle cell disease, glucose-6-phosphate dehydrogenase (G6PD) deficiency and cytochrome b5 reductase 3 (CYB5R3) T117S and ferroportin Q248H polymorphisms. G6PD, an X-linked gene, encodes the sole enzyme in red blood cells that produces NADPH for protection from reactive oxygen species. Hemi- or homozygosity for G6PD A+ (G6PD c. 376G) is an African specific polymorphism with reduced activity (PMID:26633385) but no apparent phenotype; hemi- or homozygosity for G6PD A- (G6PD c 202A/376G) is associated with both decreased activity and increased risk for oxidant-induced hemolysis (PMID:27040960). A Malaria Genomic Epidemiology Network (MalariaGEN) study with almost 30,000 participants reported that G6PD A- increases the risk for severe malarial anemia (PMID:25261933). CYB5R3 in red blood cells transfers electrons from NADH to cytochrome b5, which in turn converts methemoglobin to hemoglobin. The African-specific CYB5R3 T117S variant, is not associated with methemoglobinemia (PMID:9048929) but may afford some protection from malarial anemia in Zambian children. A prevalent African-specific Q248H mutation of the iron exporter, ferroportin, may protect from high malarial parasitemia (PMID: 29599243). We genotyped 212 Nigerian children (age 4 months - 16 years) for these genetic factors: 117 were asymptomatic children who were studied in the community and 95 were children who were studied at the time of admission to hospital with severe malaria (severe anemia and/or cerebral malaria). We isolated DNA from dried blood spots and crude DNA lysate was used for Taqman genotyping to screen for G6PD A+, G6PD A-, FPN Q248H, sickle cell disease and CYB5R3 T117S and multiplex PCR was used to identify the 3.7 kb and 4.2 kb α-globin gene deletions. The clinical characteristics of the two groups of children are shown in Table 1. Children with severe malaria were significantly younger than the children from the community. The gene frequency of CYB5R3 T117S was 0.303, of hemoglobin S was 0.094, and of FPN Q248H was 0.062. The prevalences of hemizygous and homozygous G6PD A+ and A- were 13.9% and 16.0%, respectively. In addition, the prevalences of single and double alpha globin gene deletions were 34.7 % and 11.7%, respectively. Table 2 compares the prevalence of these genotypes in asymptomatic children versus those admitted with severe malaria. Alpha-thalassemia tended to be more prevalent in the asymptomatic children while ferroportin Q248H and G6PD A- were more prevalent in the children with severe malaria. Some genes seemed to have heterogenous associations: sickle trait and homozygous CYB5R3 T117S tended to be more prevalent in the asymptomatic children while hemoglobin SS and heterozygous T117S tended to be more prevalent in the children with severe malaria. In a logistic regression model that adjusted for age, alpha thalassemia (odds ratio 0.6, P=0.038), hemoglobin S trait (odds ratio 0.5, P=0.203), and CYB5R3 T117S homozygous state (odds ratio 0.5, P=0.211) independently decreased the risk of severe malaria, while ferroportin Q248H (odds ratio 5.1, P=0.008) and G6PD deficiency (1.6, P=0.049) independently increased the risk of severe malaria. In conclusion, our results suggest that common genetic factors affect the risk of severe malaria in children. Research to illuminate the mechanisms of these effects may enhance our understanding of the pathogenesis of severe malaria and point to novel preventive and therapeutic measures. Disclosures Gordeuk: Global Blood Therapeutics: Consultancy, Honoraria, Research Funding; Emmaus: Consultancy, Honoraria; Novartis: Consultancy, Honoraria, Research Funding; Modus Therapeutics: Consultancy, Honoraria; Pfizer: Research Funding; Inctye: Research Funding; CSL Behring: Consultancy, Honoraria, Research Funding; Ironwood: Research Funding; Imara: Research Funding.

Published
2019

6. A Worldwide Map of Plasmodium falciparum K13-Propeller Polymorphisms

Author

Benoit Witkowski, Hans-Peter Fuehrer, Garib Das Thakur, Céline Barnadas, Djibrine Djalle, Michael Ramharter, Mindy Leelawong, Wasif Ali-Khan, Harald Noedl, Bouasy Hongvanthong, Mohammad Shafiul-Alam, Hypolite Muhindo-Mavoko, Abdillahi Mohamed Hassan, Judith Straimer, Nimol Khim, Kigbafori D. Silué, Kaknika Loch, Barbara H. Stokes, Maria Dorina Bustos, Laura Berne, Dylan R. Pillai, Ayola A. Adegnika, Lin Hua Tang, Rotha Eam, Saorin Kim, Alioune Dieye, Mei Li, Carole E. Eboumbou-Moukoko, Lydie Canier, Marian Warsame, Didier Menard, David A. Fidock, Yap Boum, Lyndes Wini, Abdiqani Sheikh-Omar, Patrick Tshibangu-Wa-Tshibangu, Maman Laminou Ibrahim, Mohammad Jahirul-Karim, Malen Ken, Monique A. Dorkenoo, Sócrates Herrera, Odile Mercereau-Puijalon, Lise Musset, Valentine Duru, Eric Legrand, Maniphone Khanthavong, Pascal Ringwald, Bruno Pradines, Sandrine Houzé, Rachida Tahar, Olukemi K. Amodu, Johann Beghain, Sandie Menard, Liwang Cui, Colin J. Sutherland, Jun Hu Chen, Kesara Na-Bangchang, Khin Lin, Michael Nambozi, Rithea Leang, Jean Christophe Barale, Milijaona Randrianarivelojosia, Marcus V. G. Lacerda, Sophy Chy, Frédéric Ariey, Jean-Bosco Ouédraogo, Isabelle Morlais, Maria de Fátima Ferreira-da-Cruz, Lubin Jiang, Christophe Rogier, Jun Cao, Peter G. Kremsner, Bui Quang-Phuc, Inès Vigan-Womas, Din Syafruddin, Jetsumon Sattabongkot, Shigeyuki Kano, Abebe A. Fola, Louis Collet, Karamoko Niaré, Thierry Fandeur, Sedigheh Zakeri, Sodiomon B. Sirima, Antoine Berry, Jean Baptiste Mazarati, Fe Espino, Ghulam Rahim-Awab, Chanra Khean, Offianan Andre Toure, Institut Pasteur du Cambodge, Réseau International des Instituts Pasteur (RIIP), Génétique et Génomique des Insectes vecteurs, Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS), Eberhard Karls Universität Tübingen = Eberhard Karls University of Tuebingen, Centre de Recherche Médicale de Lambaréné, Albert Schweitzer, Leiden University Medical Center (LUMC), Universiteit Leiden, International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR,B), University of Ibadan, Nangarhar University, Mahidol University [Bangkok], The Walter and Eliza Hall Institute of Medical Research (WEHI), University of Melbourne, Papua New Guinea Institute for Medical Research (PNGIMR), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Mbarara University of Science and Technology [Mbarara] (MUST), Epicentre Ouganda [Mbarara] [Médecins Sans Frontières], Epicentre [Paris] [Médecins Sans Frontières], World Health Organization (WHO), country office for Thailand, Organisation Mondiale de la Santé / World Health Organization Office (OMS / WHO), JiangSu University, National Institute of Parasitic Diseases, Center for Disease Control, China, Centre Hospitalier de Mayotte, Pennsylvania State University (Penn State), Penn State System, Epidemiology and Disease Control division (EDCD), Ministry of Public Health [Nepal], Institut Pasteur de Dakar, Université Cheikh Anta Diop [Dakar, Sénégal] (UCAD), Institut Pasteur de Bangui, Université de Lomé [Togo], Université de Douala, Centre Pasteur du Cameroun, Research Institute for Tropical Medicine, Centre International de Recherches Médicales de Franceville (CIRMF), Fundação Oswaldo Cruz / Oswaldo Cruz Foundation (FIOCRUZ), University of Gondar, Institute of Parasitology [Vienna], University of Veterinary Medicine, Vienna, World Health Organisation (WHO), country office for Somalia, Caucaseco scientific research center = Centro de Investigación Científica Caucaseco, National Center for Malariology, Parasitology and Entomology, Ministry of Health [Mozambique], Hôpital Bichat - Claude Bernard, Mère et enfant en milieu tropical : pathogènes, système de santé et transition épidémiologique (MERIT - UMR_D 216), Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5), Centre de Recherche Médicale et Sanitaire (Niamey, Niger) (CERMES), Directorate General of Health Services (DGHS), Institut Pasteur de Shanghai, Académie des Sciences de Chine - Chinese Academy of Sciences (IPS-CAS), National Center for Global Health and Medicine [Japan] (NCGM), Institut Pasteur du Laos, Instituto Leônidas e Maria Deane - Fiocruz Amazônia [Manaus, Brésil] (ILMD), Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Fundação de Medicina Tropical Doutor Heitor Vieira Dourado (FMT-HVD), National Center for Malaria Control, Parasitology and Entomology, Ministry of Health of Cambodgia, Henry M. Jackson Foundation for the Advancement of Military Medicine (HJM), U.S. Naval Medical Research, The Department of Medical Research (Upper Myanmar), Rwanda Biomedical Center (RBC), Centre de Physiopathologie Toulouse Purpan (CPTP), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de Recherche pour le Développement [Yaoundé, Cameroun] (IRD [Cameroun]), Institut de Recherche pour le Développement (IRD), University of Kinshasa (UNIKIN), University of Antwerp (UA), Institut Pasteur de la Guyane, Thammasat University (TU), Tropical Diseases Research Center (TDRC), Université de Bamako, Medizinische Universität Wien = Medical University of Vienna, Institut de Recherche en Sciences de la Santé (IRSS) / Centre Muraz, Medicines for Malaria Venture (MMV), Université de Genève = University of Geneva (UNIGE), Global Malaria Programme, Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes (URMITE), Institut de Recherche pour le Développement (IRD)-Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR48, Institut des sciences biologiques (INSB-CNRS)-Institut des sciences biologiques (INSB-CNRS)-Centre National de la Recherche Scientifique (CNRS), Centre National de Référence du Paludisme, Institut Pasteur de Madagascar, Ministry of Health and Human Services [Somalia], Centre Suisse de Recherches Scientifiques en Cote d'Ivoire [Abidjan] (CSRS-CI), Université Félix Houphouët-Boigny (UFHB), Groupe de recherche action en santé (GRAS), London School of Hygiene and Tropical Medicine (LSHTM), University of Hasanuddin, Eijkman Institute for Molecular Biology [Jakarta], Institut Pasteur de Côte d'Ivoire, Ministry of Health and Medical Services, Institut Pasteur d'Iran, Centre National de Référence du Paludisme [Cayenne, Guyane française] (CNR - laboratoire associé), Microbiologie structurale - Structural Microbiology (Microb. Struc. (UMR_3528 / U-Pasteur_5)), Institut Pasteur [Paris] (IP)-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Columbia University Irving Medical Center (CUIMC), Institut de Recherche Biomédicale des Armées [Antenne Marseille] (IRBA), AP-HP - Hôpital Cochin Broca Hôtel Dieu [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Descartes - Paris 5 (UPD5), Supported by the Institut Pasteur Paris, Institut Pasteur International Division, Institut Pasteur Cambodia, and the World Health Organization, by a grant (ANR-10-LABX-62-IBEID) from the French Government Investissement d’Avenir program, Laboratoire d’Excellence 'Integrative Biology of Emerging Infectious Diseases', a grant from Natixis Banques, a grant (R01I109023, to Dr. Fidock) from the National Institutes of Health, grants from the Fiocruz Fundação Oswaldo Cruz, Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro, Fundação de Amparo à Pesquisa do Estado do Amazonas, the Brazilian National Council for Scientific and Technological Development, the Agence Nationale de la Recherche (13-BSV3-0018-01 and11-BSV7-009-01), the Austrian Federal Ministry of Science, Research, and Econo-my, the Calgary Laboratory Services, the Centre International de Recherches Médicales de Franceville, the European and Developing Countries Clinical Trials Partnership (CT-2004-31070-001), the Drugs for Neglected Diseases Initiative, the Else Kroener Fresenius Stiftung, the Holger Poehlmann Stiftung, the European Community African–European Research Initiative 'IDEA' (HEALTH-F3-2009-241642), the Fonds Wetenschappelijk Onderzoek, the Vlaamse Interuniversitaire Raad–Universitaire Ontwikkelingssamenwerking, the Belgian Technical Cooperation in Democratic Republic of Congo, the European Community Seventh Framework Program (FP7/2007-2013, 242095, and 223601), the European Commission (REGPOT-CT-2011-285837-STRONGER), the Ministère de la Santé Publique du Niger (Laboratoire National de Référence Résistance aux Antipaludiques), the Foundation of National Science and Technology Major Program (2012ZX10004-220), the French Ministry of Health (Institut National de Veille Sanitaire), the Global Fund to Fight AIDS, Tuberculosis and Malaria, the 5% Initiative program (French Ministry of Foreign Affairs, France Expertise Internationale, 12INI109), the Institut Pasteur de Madagascar, the Government of the Philippines, the Institut de Recherche pour le Développement, the Foundation des Treilles, the Délégation Générale pour l’Armement (PDH-2-NRBC-4-B1-402), the Institut Pasteur de Bangui, the International Society for Health Research and Training, the Malaria Research Initiative Bandarban, Vienna, International Centre for Diarrhoeal Disease Research, Bangladesh, the Médecins sans Frontières (Centre Opérationnel Paris, France), Medicines for Malaria Venture, the National Research Council of Thailand, the Thammasat University, the National Natural Science Foundation of China (81271870, 81361120405, and 81271863), the Natural Science Foundation of Jiangsu Province (BK20130114 and BK20150001), the Jiangsu Science and Technology Department (BM2015024), the National Institutes of Health (R01 AI11646601, AI109023, and ICEMR U19AI089702, U19AI089672), the Pasteur Institute of Iran, the Malaria Division of the Iranian Center for Diseases Management and Control, Public Health England (Malaria Reference Service Contract), the Government of Rwanda, the U.S. Department of Defense Armed Forces Health Surveillance Center, Global Emerging Infections Surveillance and Response System (P0463-14-N6), the Fogarty International Center of the National Institutes of Health training (D43 TW007393), the Mahidol-Oxford Research Unit, the Government of Japan (Science and Technology Agency, Agency for Medical Research and Development, Japan International Cooperation Agency, and Science and Technology Research Partnership for Sustainable Development), and the President’s Malaria Initiative of the U.S. Agency for International Development., The KARMA Consortium, ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), ANR-13-BSV3-0018,MALARTRES,Résistance de Plasmodium aux antipaludiques de la famille des artémisinines(2013), ANR-13-BSV7-0009,NEBEDIV,Le rôle des ennemis naturels dans la diversité béta des arbres tropicaux(2013), European Project: CT-2004-31070-001,EDCCTP, European Project: HEALTH-F3-2009-24164,IDEA, European Project: FP7/2007-2013, 24209,FP7, European Project: FP7/2007-2013, 22360,FP7, European Project: 285837,EC:FP7:REGPOT,FP7-REGPOT-2011-1,STRONGER(2011), European Project: 242095,EC:FP7:HEALTH,FP7-HEALTH-2009-single-stage,EVIMALAR(2009), European Project: 223601,EC:FP7:HEALTH,FP7-HEALTH-2007-B,MALVECBLOK(2009), Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), CHU Toulouse [Toulouse], Fundação Oswaldo Cruz (FIOCRUZ), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Genève (UNIGE), INSB-INSB-Centre National de la Recherche Scientifique (CNRS), Centre National de Référence du Paludisme [Cayenne, Guyane française] (CNR), Université Paris Diderot - Paris 7 (UPD7)-Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Eberhard Karls Universität Tübingen, The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia., Centre International de Recherches Médicales de Franceville, Caucaseco scientific research center, Mère et enfant face aux infections tropicales (MERIT - UMR_D 216), National Center for Global Health and Medicine (NCGM), Instituto Leônidas e Maria Deane (ILMD), Centre de Physiopathologie Toulouse Purpan ex IFR 30 et IFR 150 (CPTP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Institut de Recherche pour le Développement [Yaoundé], Centre Suisse de Recherches Scientifiques en Côte d'Ivoire, Eijkman Institute for Molecular Biology, Laboratoire de Parasitologie, Centre National de Référence du Paludisme - Région Antilles-Guyane, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-WHO Collaborating Center for Surveillance of Antimalarial Drug Resistance, Institut Pasteur [Paris]-Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), ANR-10-LABX-62-IBEID,IBEID,Laboratoire d'Excellence 'Integrative Biology of Emerging Infectious Diseases'(2010), Van geertruyden, Jean-Pierre, and KARMA Consortium

Subjects
0301 basic medicine, Nonsynonymous substitution, MESH: Sequence Analysis, DNA, Endemic Diseases, MESH: Asia, Southeastern, Drug Resistance, Protozoan Proteins, Drug resistance, MESH: Genotype, Lactones, 0302 clinical medicine, Genotype, Artemisinin, Malaria, Falciparum, MESH: Protozoan Proteins, Asia, Southeastern, MESH: Plasmodium falciparum, Genetics, biology, MESH: Malaria, Falciparum, General Medicine, Artemisinins, MESH: China, 3. Good health, MESH: Endemic Diseases, MESH: Drug Resistance, Algorithms, MESH: Lactones, medicine.drug, China, MESH: Mutation, 030231 tropical medicine, 030106 microbiology, Plasmodium falciparum, MESH: Algorithms, 03 medical and health sciences, parasitic diseases, MESH: Artemisinins, MESH: Polymorphism, Genetic, medicine, Humans, [SDV.MP.PAR]Life Sciences [q-bio]/Microbiology and Parasitology/Parasitology, Allele, Polymorphism, Genetic, MESH: Humans, Haplotype, Sequence Analysis, DNA, medicine.disease, biology.organism_classification, Virology, Mutation, Human medicine, Malaria
Abstract

Comment inK13-Propeller Mutations and Malaria Resistance, http://www.nejm.org/doi/full/10.1056/NEJMe1604520; International audience; BACKGROUND:Recent gains in reducing the global burden of malaria are threatened by the emergence of Plasmodium falciparum resistance to artemisinins. The discovery that mutations in portions of a P. falciparum gene encoding kelch (K13)-propeller domains are the major determinant of resistance has provided opportunities for monitoring such resistance on a global scale.METHODS:We analyzed the K13-propeller sequence polymorphism in 14,037 samples collected in 59 countries in which malaria is endemic. Most of the samples (84.5%) were obtained from patients who were treated at sentinel sites used for nationwide surveillance of antimalarial resistance. We evaluated the emergence and dissemination of mutations by haplotyping neighboring loci.RESULTS:We identified 108 nonsynonymous K13 mutations, which showed marked geographic disparity in their frequency and distribution. In Asia, 36.5% of the K13 mutations were distributed within two areas--one in Cambodia, Vietnam, and Laos and the other in western Thailand, Myanmar, and China--with no overlap. In Africa, we observed a broad array of rare nonsynonymous mutations that were not associated with delayed parasite clearance. The gene-edited Dd2 transgenic line with the A578S mutation, which expresses the most frequently observed African allele, was found to be susceptible to artemisinin in vitro on a ring-stage survival assay.CONCLUSIONS:No evidence of artemisinin resistance was found outside Southeast Asia and China, where resistance-associated K13 mutations were confined. The common African A578S allele was not associated with clinical or in vitro resistance to artemisinin, and many African mutations appear to be neutral. (Funded by Institut Pasteur Paris and others.).

Published
2016

7. Complexity of themsp2locus and the severity of childhood malaria, in south–western Nigeria

Author

Segun I. Oyedeji, F. Ntoumi, Adebola E. Orimadegun, O. O. Omotade, P.E. Olumese, Olukemi K. Amodu, and Rasheed Gbadegesin

Subjects
Male, medicine.medical_specialty, Endemic Diseases, Genotype, Plasmodium falciparum, Population, Malaria, Cerebral, Protozoan Proteins, Nigeria, Antigens, Protozoan, Severity of Illness Index, Asymptomatic, Internal medicine, parasitic diseases, Severity of illness, medicine, Animals, Humans, Malaria, Falciparum, education, Alleles, Merozoite Surface Protein 1, education.field_of_study, biology, Genetic Variation, Infant, Anemia, medicine.disease, biology.organism_classification, Infectious Diseases, Cerebral Malaria, Child, Preschool, Tropical medicine, Immunology, Female, Parasitology, medicine.symptom, Malaria
Abstract

As the genetic diversity of Plasmodium falciparum infections in humans is implicated in the pathogenesis of malaria, the association between P. falciparum diversity at the merozoite surface protein-2 (msp2) locus and the severity of childhood malaria was investigated in Ibadan, in south-western Nigeria. The 400 children enrolled had acute uncomplicated malaria (144), cerebral malaria (64), severe malarial anaemia (67) or asymptomatic infections with P. falciparum (125). Nested PCR was used to investigate the msp2 genotype(s) of the parasites infecting each child. In terms of the complexity of infection and frequency of polyinfection, the children with asymptomatic infection were significantly different from those with uncomplicated malaria or severe malaria. The median number of FC27 alleles detected was higher in the asymptomatic children than in the symptomatic. After controlling for age and level of parasitaemia (with 'asymptomatic infection' as the reference category), a child in whom no FC27 alleles were detected was found to be at five-fold greater risk of uncomplicated malaria, and a child without polyinfection was found to have a three-fold increased risk of severe malarial anaemia and a six-fold increased risk of cerebral malaria. It therefore appears that msp2 genotypes are associated with asymptomatic carriage and that children with mono-infections are more likely to develop severe malaria than children with polyinfection.

Published
2008

8. Plasmodium falciparum malaria in south-west Nigerian children: Is the polymorphism of ICAM-1 and E-selectin genes contributing to the clinical severity of malaria?

Author

A.K. Akinsola, P.E. Olumese, S.A. Ralph, Paul Brenchley, Rasheed Gbadegesin, Olukemi K. Amodu, Adebowale Adeyemo, O.O. Ayoola, Adebola E. Orimadegun, and O. O. Omotade

Subjects
Male, Veterinary (miscellaneous), Nigeria, Locus (genetics), Severity of Illness Index, Apicomplexa, Loss of heterozygosity, Exon, parasitic diseases, medicine, Humans, Malaria, Falciparum, Allele, Genotyping, Genetics, Polymorphism, Genetic, biology, Plasmodium falciparum, Intercellular Adhesion Molecule-1, biology.organism_classification, medicine.disease, Infectious Diseases, Child, Preschool, Insect Science, Immunology, Female, Parasitology, E-Selectin, Malaria
Abstract

Plasmodium falciparum malaria remains a major public health hazard in sub-Saharan African children. While the factors that determine the variations in clinical outcome of a malaria have not been completely defined, both host and parasite factors, as well as the complex molecular interactions between them have been implicated. The cyto-adherent properties of the P. falciparum -infected red blood cells are considered as key properties in the pathogenesis of malaria and the polymorphisms of the host adhesion molecules could contribute to the severity of malaria. Clinical information and blood samples were collected from 223 children from Ibadan (south-west Nigeria), median age of 34.5 months, presenting with different clinical manifestations of malaria—clinically asymptomatic parasitism (ACP), acute uncomplicated malaria (UM) and severe malaria (SM)—as defined by WHO criteria. The polymorphisms of genes coding for four human adhesion molecules at six different loci (ICAM-1 exons 2, 4 and 6, E-selectin exon 2, CD36 exon 10, and PECAM exon 3) were studied. DNA samples were prepared for further genotyping of the six exons mentioned above by PCR-RFLPs using the appropriate restriction digests for each loci. The ICAM-1 exon 4 locus was monomorphic. All the other loci were at Hardy-Weinberg equilibrium (HWE).The E-selectin locus had very low heterozygosity (∼0.06) in contrast to the other loci under study (0.23–0.44). Once the data was further processed for covariates (age and parasite density) and taking as the reference category the ACP group, results show that in the presence of the G allele at the ICAM-1 exon 6 there is an increased risk (3.6 times) of severe malaria. As far as the T allele in the E-selectin exon is concerned, the number of sampled DNAs with the T allele within both the UM and SM categories is too low for drawing any relevant conclusion at this stage. In conclusion, these results suggest that genetic polymorphisms at host adhesion molecules loci are an important variable in the susceptibility to severe malaria. Further studies of host loci are needed to further delineate which polymorphisms are associated with severe malaria and increase our knowledge of the biology of host-parasite interactions.

Published
2005

9. Enabling the genomic revolution in Africa

Author

Anh Quynh Nguyen, Daniel T. Lackland, Gustave Simo, Oumar Samassekou, Lukman Owolabi, Faisal M. Fadlelmola, Matthias Kretzler, Victoria Adabayeri, Jeffrey B. Kopp, Mary T Mayige, Mark S. Guyer, Charlotte Osafo, Nigel J. Crowther, Winston Hide, Eyitayo Fakunle, Guillaume Paré, Issa Sidibe, Bamidele O. Tayo, Manmak Mamven, Stephen Tollman, Christian T. Happi, Anne Fischer, James A. G. Whitworth, Andrew Tareila, Moses Joloba, Kristian G. Andersen, Odile Ouwe Missi Oukem-Boyer, Paul L. Kimmel, Thuli Mthiyane, Anita Ghansah, Sylvester Leonard Lyantagaye, T O Olanrewaju, John Enyaru, Kwamena W. Sagoe, Maia Lesosky, Neil A. Hanchard, Rita T. Lawlor, Ellis Owusu-Dabo, Eileen Obe, Shiksha Reddy, Margaret B. Penno., Rembert Pieper, Maria Y. Giovanni, Louise Wideroff, Yasmina Jaufeerally-Fakim, Marape Marape, Stacy Carrington-Lawrence, Oyekanmi Nash, Dwomoa Adu, Rebekah S. Rasooly, Rajkumar Ramesar, Mukthar Kader, Carolyn Jenkins, Simani Gaseitsiwe, Michèle Ramsay, Betty Nsangi, Olukemi K. Amodu, Mark P. Nicol, Adeodata Kekitiinwa, Thomas Lehner, Nzovu Ulenga, Saidi Kapiga, Victor Jongeneel, Gebregziabher Mulugeta, Nathan L. Yozwiak, Gabriel Anabwani, Solomon F. Ofori-Acquah, Misaki Wayengera, Rasheed Bakare, Marianne Alberts, Jantina de Vries, Robert F. Garry, Marsha Treadwell, Robert Kleta, Eugene Sobngwi, Ezra Susser, Mo Nagdee, Carmen Swanepoel, Osman Sankoh, Masego Tsimako-Johnstone, Godfred Tangwa, Zané Lombard, Darren P. Martin, Donald S. Grant, Bernard Keavney, Mahamadou Traoré, Ahmed El Sayed, Seth O. McLigeyo, Charles Mondo, Dan J. Stein, Özlem Tastan Bishop, Jane Peterson, Ute Jentsch, Moffat Nyirenda, Charles N. Rotimi, Shane A. Norris, Chengetai R. Mahomva., Gobena Ameni, Sheryl A. McCurdy, M Boehnke, Sally N Akarolo-Anthony, Oumou Sow Bah, Muntaser E. Ibrahim, Ishmael Kasvosve, Dean Everett, Kathleen Kahn, S.W.O. Ogendo, Abraham Oduro, Cheryl A. Winkler, Robin Mason, Orlando Alonso Betancourt, Hugh-G. Patterton, Heather J. Zar, John Oli, Audrey Duncanson, Daouda Ndiaye, Alan Christoffels, Adebowale Adeyemo, Kenneth H. Fischbeck, Manjinder S. Sandhu, Kwaku Ohene-Frempong, Samuel Ajayi, Chester W. Brown, Godfred Agongo, Tunde Salako, Ablo Prudence Wachinou, Gasnat Shaboodien, Pardis C. Sabeti, Jean Claude Mbanya, Peter Donkor, Dieuodonne Mumba, Heather J. Cordell, Sarah Winnicki, Reginald Obiakor, Fourie Joubert, Samar K. Kassim, Mark I. McCarthy, Scott Hazelhurst, Pontiano Kaleebu, Richard S. Cooper, Jennifer L. Troyer, Hermann Sorgho, Oyedunni Arulogun, Ravnit Grewal, Bongani M. Mayosi, Jacob Plange-Rhule, Christiane Hertz-Fowler, Alia Benkahla, Okechukwu S Ogah, Akin Abayomi, Mayowa O. Owolabi, Mark E Engel, Rufus Akinyemi, Ezekiel Adebiyi, Alash'le Abimiku, John Chisi, Patricia A. Marshall, Bruce Ovbiagele, Catherine Kyobutungi, Ambroise Wonkam, Vincent Tukei, David T. Burke, Fred Stephen Sarfo, Andrew Owen, Julie Makani, Leslie Derr, Mary Claire King, Nicki Tiffin, Vincent Boima, Barrington G. Burnett, Martin Simuunza, Christine Beiswanger, Nicola Mulder, Ekaete Tobin, Katherine Littler, Frank C. Brosius, Rulan S. Parekh, Halidou Tinto, Talishiea Croxton, Onikepe A. Folarin, Seydou Doumbia, Parham Goesbeck, Salina P. Waddy, Andrew Brooks, Marva Moxey-Mims, Guida Landouré, Marie Sarr, Martin R. Pollak, Akinlolu O. Ojo, Danny Asogun, Beverley van Rooyen, Clement Adebamowo, Jeanne F. Loring, Naomi S. Levitt, Jonathan K. Kayondo, Nadia Carstens, John V. Moran, F. Xavier Gómez-Olivé, John Musuku, Enock Matovu, Ifeoma Ulasi, Alisha N. Wade, Regina James, Ebony B. Madden, Liam Smeeth, Friedhelm Hilderbrandt, James Brandful, Chisomo L. Msefula, Christopher Hugo-Hamman, Annette MacLeod, Lara Bethke, Judit Kumuthini, Julia Puzak, Mengistu Tadase Yewondwossen, Sudha Srinivasan, Sheik Humarr Khan, Daniel K. Masiga, Mathurin Koffi, Oathokwa Nkomazana, Sununguko Wata Mpoloka, Fatiu A Arogundade, Dissou Affolabi, Ahmed M. Alzohairy, Ayesha A. Motala, Pan Pan Jiang, Adebowale D. Ademola, Ana Olga Mocumbi, Samuel Kyobe, Graeme Mardon, Albert Akpalu, Karen A. Lacourciere, Himla Soodyall, Branwen J. Hennig, Bruno Bucheton, Naby Balde, Michael Mate-Kole, Alexander K. Nyarko, Helen McIlleron, Mary Lynn Baniecki, Ivy Ekem, Corrine Merle, Rasheed Gbadegesin, Junaid Gamieldien, Makerere University [Kampala, Ouganda] (MAK), Institut de Recherche pour le Développement (IRD), University of Malawi, University of Liverpool, Université Jean Lorougnon Guédé (UJloG ), University of Glasgow, Institut National de Recherche Biomédicale [Kinshasa] (INRB), Centre international de recherche-développement sur l'élevage en zone sub-humide (CIRDES), Université de Dschang, University of Zambia [Lusaka] (UNZA), University of Cape Town, University of Nairobi (UoN), Instituto Nacional de Saude [Maputo, Mozambique] (INS), Windhoek Central Hospital [Namibie], University College Hospital [Ibadan, Nigeria], Alzaiem Alazhari University [Soudan] (AAU-Sudan), Mulago Hospital [Kampala, Ouganda], Newcastle University [Newcastle], McMaster University [Hamilton, Ontario], University of Manchester [Manchester], Nelson R Mandela School of Medicine [Durban, South Africa] (NRMSM), University of KwaZulu-Natal (UKZN), University of Yaoundé [Cameroun], Medical Research Council Unit The Gambia (MRC), Hôpital Donka, Ministère de la Santé [Conakry, Guinea], Malawi Liverpool Wellcome Trust Clinical Research Programme (MLW), Liverpool School of Tropical Medicine (LSTM)-University of Liverpool-Wellcome Trust-University of Malawi, University of Nigeria, Institute of Human Virology [Nigeria] (IHVN), National Institute for Medical Research [Tanzania] (NIMR), MRC/UVRI & LSHTM Uganda Research Unit, Medical Research Council-London School of Hygiene and Tropical Medicine (LSHTM)-Medical Research Council Unit The Gambia (MRC)-Uganda Virus Research Institute (UVRI), The Wellcome Trust Sanger Institute [Cambridge], London School of Hygiene and Tropical Medicine (LSHTM), Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM), University of Oxford [Oxford], The Wellcome Trust Centre for Human Genetics [Oxford], National Human Genome Research Institute (NHGRI), Institut Pasteur de Tunis, and Réseau International des Instituts Pasteur (RIIP)

Subjects
MESH: Health, [SDV]Life Sciences [q-bio], MEDLINE, Genomics, Genome-wide association study, Computational biology, Biology, MESH: Africa, 03 medical and health sciences, 0302 clinical medicine, MESH: England, Research capacity, MESH: Disease/genetics, MESH: United States, 030212 general & internal medicine, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, Multidisciplinary, MESH: Humans, business.industry, MESH: Genomics/trends, Biotechnology, MESH: Genome-Wide Association Study/trends, MESH: Genetics, Medical/trends, business, MESH: National Institutes of Health (U.S.)
Abstract

H3Africa is developing capacity for health-related genomics research in Africa

Published
2014

10. Chloroquine resistance of Plasmodium falciparum is associated with severity of disease in Nigerian children

Author

Anders Björkman, Adebowale Adeyemo, O. Walker, P.E. Olumese, Rasheed Gbadegesin, and Olukemi K. Amodu

Subjects
Male, Plasmodium falciparum, Drug Resistance, Nigeria, Virulence, macromolecular substances, Disease, Pathogenesis, Antimalarials, Chloroquine, parasitic diseases, Severity of illness, medicine, Animals, Humans, Risk factor, Child, biology, Public Health, Environmental and Occupational Health, Infant, General Medicine, biology.organism_classification, medicine.disease, Infectious Diseases, Child, Preschool, Immunology, Regression Analysis, Female, Parasitology, Malaria, medicine.drug
Abstract

Chloroquine resistance of Plasmodium falciparum in vitro was significantly higher in isolates from patients with severe malaria than those with uncomplicated disease. This association may be due to either progression of uncomplicated to severe disease following chloroquine failure or increased virulence of chloroquine-resistant parasites. The implication of this for antimalarial treatment policy is discussed.

Published
2002

11. A global network for investigating the genomic epidemiology of malaria

Author

Julie Makani, Kathryn Fitzpatrick, Ogobara K. Duombo, Jennifer Evans, Claire Potter, Giorgio Sirugo, Enmoore Lin, Christina Hubbart, Abier Elzein, Martha M. Lemnge, Anthony Enimil, Alioune Ly, Olukemi K. Amodu, Valentina D. Mangano, Angie Green, Alphaxard Manjurano, Dominic P. Kwiatkowski, Ivo Mueller, David Barnwell, Anna E. Jeffreys, Marryat Stevens, Thomas N. Williams, David Modiano, Sarah J. Dunstan, Taane G. Clark, Susana Campino, Tobias O. Apinjoh, Tran Tinh Hien, Sodiomon B. Sirima, David J. Conway, Terrie Taylor, Anavaj Sakuntabhai, L. Amenga-Etego, Catherine L. Moyes, Nguyen Ngoc Quyen, Laurens Manning, Mahamadou Diakite, Katharine Cook, Patrick H. Corran, Jeremy Farrar, Nadira D. Karunaweera, Kevin Marsh, Ogobara K. Doumbo, Catherine Hughes, Eric A. Achidi, Kirk A. Rockett, Chris Drakeley, Tsiri Agbenyega, Panos Deloukas, Mahamadou A. Thera, Kalifa Bojang, Julie Evans, Aaron Vanderwal, Christopher V. Plowe, Pascal Michon, Adama Tall, Aceme Nyika, Michael Gottlieb, Renee Watson, Gilbert Kokwaro, Jiannis Ragoussis, Eleanor M. Riley, Stephen Allen, Katja Kivinen, Muntaser E. Ibrahim, Bronwyn MacInnis, Vysaul Nyirongo, Elilan Somaskantharajah, Ayman S. Hussein, Alan Doyle, Carolyne M. Ndila, Michael T. Wilson, Muminatou Jallow, Jane Rogers, Abdoulaye Djimde, Deepika Fernando, Jantina DeVries, Patrick E. Duffy, Odile Puijalon, Yik Ying Teo, Kate Rowlands, Michael W. Parker, Deus S. Ishengoma, Marilyn McCreight, Edith C. Bougouma, Tom Oluoch, Rebecca Wrigley, Kerrin S. Small, Hugh Reyburn, Gareth Maslen, Malcolm E. Molyneux, Sarah Auburn, Eliza Hilton, Lee Hart, Pratap Singhasivanon, Alieu Mendy, Miguel A. Sanjoaquin, Magnus Manske, Anita Ghansah, Rajika L. Dewasurendra, Amagana Dolo, Dan Carucci, Theonest K. Mutabingwa, Prapat Suriyaphol, Marita Troye-Blomberg, Paul Risley, Susan Bull, Rolf D. Horstmann, Daniel Alcock, Ousman Toure, Kojo Koram, John C. Reeder, and Norbert Peshu

Subjects
Burden of disease, Economic growth, medicine.medical_specialty, Plasmodium, Population, Developing country, Global Health, Polymorphism, Single Nucleotide, Article, Political science, Epidemiology, Global network, Anopheles, Global health, medicine, Animals, Humans, education, education.field_of_study, Multidisciplinary, biology, business.industry, Genome, Human, biology.organism_classification, medicine.disease, Immunity, Innate, Biotechnology, Malaria, Epidemiologic Research Design, business, Genome-Wide Association Study
Abstract

Large-scale studies of genomic variation could assist efforts to eliminate malaria. But there are scientific, ethical and practical challenges to carrying out such studies in developing countries, where the burden of disease is greatest. The Malaria Genomic Epidemiology Network (MalariaGEN) is now working to overcome these obstacles, using a consortial approach that brings together researchers from 21 countries. © 2008 Macmillan Publishers Limited. All rights reserved.

Published
2008

12. Patterns of polymorphism in genomic regions flanking three highly polymorphic surface antigens in Plasmodium falciparum

Author

Daniel L. Hartl, Olukemi K. Amodu, and Scott William Roy

Subjects
Population, Molecular Sequence Data, Plasmodium falciparum, Protozoan Proteins, Single-nucleotide polymorphism, Antigens, Protozoan, Biology, Balancing selection, Polymorphism, Single Nucleotide, Nucleotide diversity, Negative selection, parasitic diseases, Animals, Humans, education, Molecular Biology, Gene, Merozoite Surface Protein 1, Genetics, education.field_of_study, Polymorphism, Genetic, Base Sequence, Sequence Analysis, DNA, biology.organism_classification, Circumsporozoite protein, Genetics, Population, Parasitology
Abstract

Many surface antigens of the human malaria parasite Plasmodium falciparum show extraordinary diversity, with different alleles being so divergent as to be unalignable in some coding regions. To better understand the population history and modes of selection on such loci, we sequenced genomic regions flanking the highly polymorphic genes merozoite surface protein-1, merozoite surface protein-2, and circumsporozoite protein, from reference isolates of P. falciparum . Diversity was much lower in genomic flanking regions than in the coding sequences. Average pairwise nucleotide diversity for these regions was 0.00088, similar to other genomic regions not thought to be evolving under balancing selection, suggesting against balancing selection acting on promoter regions of these genes. Most observed polymorphisms were singletons. A higher ratio of SNPs to indels than previously reported for P. falciparum was observed. An 11 bp repeat upstream of msp2 showed an intriguing pattern of polymorphism possibly suggestive of purifying selection on total allele length.

Published
2007

13. Genetic diversity of the msp-1 locus and symptomatic malaria in south-west Nigeria

Author

Adebola E. Orimadegun, P.E. Olumese, A.K. Akinsola, Olukemi K. Amodu, Adebowale Adeyemo, O. O. Omotade, Rasheed Gbadegesin, and O.O. Ayoola

Subjects
Male, medicine.medical_specialty, Genotype, Veterinary (miscellaneous), Plasmodium falciparum, Nigeria, Locus (genetics), Biology, Severity of Illness Index, parasitic diseases, Severity of illness, medicine, Animals, Humans, Allele, Malaria, Falciparum, Genotyping, Merozoite Surface Protein 1, Genetic Variation, medicine.disease, biology.organism_classification, Infectious Diseases, Insect Science, Child, Preschool, Immunology, Tropical medicine, Parasitology, Female, Malaria
Abstract

Genetic characteristics of Plasmodium falciparum may play a role in the clinical severity of malaria infection. We have studied the association between diversity at the merozoite surface protein-1 (msp-1) locus and the severity of disease in childhood malaria in Ibadan, south-west Nigeria. Two hundred and twenty-three children (median age of 34.5 months) presenting with malaria were enrolled into the study. They comprised 53 children with asymptomatic malaria (ASM), 101 with acute uncomplicated malaria (UM) and 69 with severe malaria (SM). Genotyping of the msp-1 locus was by polymerase chain reaction. The distribution of msp-1 alleles was significantly different between the three groups. Asymptomatic malaria samples had a higher median number of alleles than the other two groups. The type of msp-1 allele detected was significantly associated with the clinical category of malaria. The absence of K1 alleles was associated with a three-fold increase risk of UM and a four-fold increased risk of SM when compared with asymptomatic malaria. The absence of MAD20 alleles was associated with a five-fold increase risk of UM and an eight-fold increase of SM. We have found an association between the msp-1 locus of P. falciparum and clinical severity of malaria in a sample of Nigerian children. Our findings show that the presence of the K1 and MAD20 alleles was significantly associated with ASM and consequently a reduced risk of developing the symptomatic disease.

Published
2005

14. The influence of individual preventive measures on the clinical severity of malaria among Nigerian children

Author

Olukemi K. Amodu, Adebowale Adeyemo, P.E. Olumese, Rasheed Gbadegesin, and O.O. Ayoola

Subjects
Male, medicine.medical_specialty, Insecticides, Mosquito Control, Veterinary (miscellaneous), Population, Nigeria, Disease, Environmental health, parasitic diseases, Medicine, Humans, Malaria, Falciparum, education, education.field_of_study, biology, business.industry, Transmission (medicine), Public health, Bedding and Linens, Plasmodium falciparum, biology.organism_classification, medicine.disease, Infectious Diseases, Insect Science, Vector (epidemiology), Insect Repellents, Tropical medicine, Immunology, Housing, Parasitology, Female, business, Malaria
Abstract

Falciparum malaria is a leading cause of morbidity and mortality in endemic regions of the world. In areas of intense transmission of P. falciparum children less than the age of 5 years are the most susceptible to severe malaria. The complex interactions between the parasite the human host the vector and environment or social factors may influence the outcome of a malaria infection (White & Ho 1992). Control measures have been based on wide-scale attempts at the reduction in transmission with anti-vector measures and therapeutic management of clinical disease. In sub-Saharan Africa however control is mainly focused on management of the clinical disease and more recently on the use of intermittent preventive treatment (IPT) in pregnant women. Individual preventive measures such as the use of mosquito repellants and the use of insecticide treated bed nets (ITNs) and curtains also influence the risk of host-vector contact host infection and consequently mortality especially in children susceptible to the severe forms of the disease. (excerpt)

Published
2004

15. Intraleucocytic malaria pigment and clinical severity of malaria in children

Author

Adebowale Adeyemo, Olukemi K. Amodu, P.E. Olumese, and Rasheed Gbadegesin

Subjects
Hemeproteins, medicine.medical_specialty, Adolescent, Neutrophils, Malaria, Cerebral, Monocytes, Internal medicine, parasitic diseases, Severity of illness, Medicine, Humans, Malaria, Falciparum, Child, Malaria pigment, biology, business.industry, Hemozoin, Public Health, Environmental and Occupational Health, Infant, Plasmodium falciparum, General Medicine, biology.organism_classification, medicine.disease, Prognosis, Infectious Diseases, El Niño, Cerebral Malaria, Child, Preschool, Immunology, Absolute neutrophil count, Parasitology, business, Malaria
Abstract

Intraleucocytic malaria pigment has been suggested as a measure of disease severity in malaria. We have tested this hypothesis by studying 146 children aged 6 months to 14 years in 4 categories--cerebral malaria, mild malaria, asymptomatic malaria and 'no malaria'--in Ibadan, Nigeria, an area of intense malaria transmission in Africa. Children with cerebral malaria were studied at the university hospital, those with mild malaria at 2 primary health centres and the other 2 groups were studied in a primary school. The proportion of pigment-containing neutrophils showed a clear rise across the spectrum no malaria--asymptomatic malaria--mild malaria--cerebral malaria (median values 2.0%, 6.5%, 9.0% and 27.0%, respectively; P0.0001). The proportion of pigment-containing monocytes did not differ significantly between the mild malaria, asymptomatic malaria and no malaria groups but the cerebral malaria group had a higher median value than the other 3 groups. The ratio of pigment-containing neutrophils to pigment-containing monocytes showed the same trend across the groups of subjects as was observed with the number of pigment-containing neutrophils. It is concluded that the pigment-containing neutrophil count is a simple marker of disease severity in childhood malaria in addition to the parasite count.

Published
1998

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